As described by Zhang et al.[52], MM cell lines, induced to overexpress miR-137 after its transfection, downregulated c-MET and AKT phosphorylation by targeting the microphthalmia-associated transcription factor (MITF): c-MET is in fact a direct transcriptional target of MITF, and HGF regulates its own receptor levels via MITF. This evidence concerns the gene AKT1 and Miyoshi myopathy.